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Träfflista för sökning "WFRF:(Isaksson Marléne) srt2:(2000-2004)"

Sökning: WFRF:(Isaksson Marléne) > (2000-2004)

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1.
  • Anveden, I, et al. (författare)
  • Oral prednisone suppresses allergic but not irritant patch test reactions in individuals hypersensitive to nickel
  • 2004
  • Ingår i: Contact Dermatitis. - : Wiley. - 0105-1873 .- 1600-0536. ; 50:5, s. 298-303
  • Tidskriftsartikel (refereegranskat)abstract
    • A multicentre, randomized, double-blind, crossover study was designed to investigate the effects of prednisone on allergic and irritant patch test reactions. 24 subjects with known allergy to nickel were recruited and patch tested with a nickel sulfate dilution series in aqueous solution, 5% nickel sulfate in petrolatum and 2 dilution series of the irritants nonanoic acid and sodium lauryl sulfate. The subjects were tested x2, both during treatment with prednisone 20 mg oral daily and during placebo treatment. The total number of positive nickel patch test reactions decreased significantly in patients during prednisone treatment. The threshold concentration to elicit a patch test reaction increased and the overall degree of reactivity to nickel sulfate shifted towards weaker reactions. The effect of prednisone treatment on the response to irritants was divergent with both increased and decreased numbers of reactions, although there were no statistically significant differences compared with placebo. It is concluded that oral treatment with prednisone suppresses patch test reactivity to nickel, but not to the irritants tested.
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2.
  • Broberg, A, et al. (författare)
  • Dead Sea extract sold under-the-counter
  • 2003
  • Ingår i: British Journal of Dermatology. - : Oxford University Press (OUP). - 1365-2133 .- 0007-0963. ; 149:1, s. 206-207
  • Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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  • Hindsén, Monica, et al. (författare)
  • Photoallergic contact dermatitis from ketoprofen induced by drug-contaminated personal objects
  • 2004
  • Ingår i: Journal of American Academy of Dermatology. - : Elsevier BV. - 0190-9622. ; 50:2, s. 215-219
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Photoallergic contact dermatitis from ketoprofen has been recognized since the mid-1980s. Skin reactions have been reported to continue weeks after discontinuation of ketoprofen. One reason for this could be residual ketoprofen in the skin, which has been shown in a skin biopsy specimen. Objective: We sought to report on 3 cases of photoallergic contact dermatitis from ketoprofen in topical anti-inflammatory gels and on relapses of dermatitis appearing after use of ketoprofen-contaminated objects. Methods: We patch and photopatch tested, with standard series, the anti-inflammatory gel, ketoprofen, and its ingredients in serial dilutions and extracts of personal objects. We performed chemical investigations of personal objects with thin-layer chromatography, high-pressure liquid chromatography, and gas chromatography-mass spectrometry. Results: Photoallergy was demonstrated to ketoprofen, which was detected in personal objects. Conclusion: Relapses of photoallergic contact dermatitis in patients photoallergic to ketoprofen can be induced by ketoprofen-contaminated objects such as bandages and slippers.
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  • Isaksson, Marléne (författare)
  • Clinical and experimental studies in corticosteroid contact allergy
  • 2000
  • Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
    • Corticosteroids are anti-inflammatory and anti-proliferative substances that also can induce sensitization, mainly through skin contact. In a sensitized individual, it can be hard to disclose the contact allergy at patch testing because the anti-inflammatory effect may mask the allergic contact reaction. This is primarily seen when patch testing to potent corticosteroids is performed and the reading is done early, when the anti-inflammatory effect still prevails. In this thesis I present a hypothetical model, which can explain the different situations that emerge, when the anti-inflammatory effect influences the elicitation depending on the individual degree of hypersensitivity in a sensitized subject. Some patients allergic to the corticosteroid budesonide only reacted to very low concentrations of the sensitizer at early readings. When patch testing the corticosteroid triamcinolone acetonide, concentrations 1000 to 10,000 times lower than internationally recommended resulted in allergic reactions while the recommended concentration gave negative reactions. If testing with a corticosteroid at a high concentration results in a negative patch-test reaction, lowering the concentration may result in a positive patch-test reaction. Introducing another parameter into the model, the time factor, made it possible also to explain why negative patch test reactions are sometimes seen at early readings, while the tests may turn positive on late reading occasions. Therefore, not to miss contact allergy to corticosteroids, a reading after one week in addition to an early reading is advocated. The multi-centre study showed that 25% of the allergic reactions to corticosteroids would have been missed if a late reading had not been done. The edge reaction, consisting of a blank centre representing the whole area of the test unit and surrounded by an eczematous infiltrate, is seen in some corticosteroid allergic patients when potent corticosteroids are patch-tested. This phenomenon can also be explained by the same model. If an edge reaction appears, a late reading or testing with a lower concentration should be done. I also investigated the cross-reactivity pattern for the two diastereomers of budesonide, the R and S diastereomers, and found that results concurred with the theory that the R diastereomer cross-reacts with other substances from the group to which it belongs, group B, while the S diastereomer cross-reacts not only with other group B substances but also with some esters of group D. No inhibition of the patch test reactions was observed when patch testing the corticosteroid tixocortol pivalate and potentially cross-reacting substances at high concentrations. Aldehydes of corticosteroids are thought to be intermediates in the sensitization process. The aldehyde of hydrocortisone was therefore tested in subjects allergic to hydrocortisone. Patients reacting to hydrocortisone also reacted to the aldehyde, speaking in favour of the aldehyde being an intermediate in the sensitization. When trying to elucidate whether a corticosteroid mix, consisting of the three corticosteroids budesonide, tixocortol pivalate and hydrocortisone-17-butyrate (Hc-17-B) in petrolatum, could disclose corticosteroid allergy I found that 60% of the patients allergic to tixocortol pivalate were missed. Thus, in a corticosteroid mix containing budesonide and Hc-17-B, tixocortol pivalate should not be a part. Of the separate markers that were patch-tested simultaneously in petrolatum, budesonide 0.10% detected most allergic subjects, followed by budesonide 0.002% and tixocortol pivalate, both concentrations (1.0% and 0.10%) detecting the same number of patients. Hc-17-B at 1.0% detected more than 0.10%. Investigations on the stability of budesonide, tixocortol pivalate and Hc-17-B patch-test preparations in petrolatum disclosed that these were stable for at least one year in room temperature, refrigerated and frozen. Budesonide and tixocortol pivalate in ethanol showed the same stability. Hc-17-B 1.0% in ethanol was only stable frozen for one year and at room temperature for three months. In the study on local clinical relevance, the flare-up reactions in the budesonide-allergic individuals consisted not only of a severe deterioration of the Preferid® treated eczema but also toxicoderma-like eruptions with a conspicuous distribution. A correlation was found between contact allergy to budesonide and deterioration of the eczema treated with Preferid® cream containing budesonide. To study flare-up reactions at earlier budesonide test sites a systemic provocation with Pulmicort® Turbuhaler® (budesonide) via inhalation was performed in subjects allergic to budesonide but without asthma or other lung dysfunction. The study clearly showed that flare-up reactions were found after normal doses of budesonide. Therefore, a person hypersensitive to budesonide should not be given the drug as an inhalant. In the same study a new method in humans to test for cross-sensitivity was used. When budesonide was inhaled, a flare-up was noted where triamcinolone acetonide had been tested previously, indicating cross-reactivity between budesonide and triamcinolone acetonide.
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